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肝脏内质网异常的突变小鼠中的血清蛋白合成

Serum protein synthesis in mutant mice with abnormal hepatic endoplasmic reticulum.

作者信息

Erickson R P, Pickart L, Thaler M M

出版信息

Cytobios. 1976;15(57):49-56.

PMID:63355
Abstract

Severe ultrastructural abnormalities of liver endoplasmic reticulum have been described in newborn mice homozygous for radiation-induced deletion alleles at the colour locus. The ultrastructural defects were accompanied by deficiencies of several enzymes and lowered serum protein levels. Studies on serum protein synthesis were undertaken to see if decreased rates of synthesis, especially of constituents thought to be synthesized on membrane-bound ribosomes, were the cause of the deficiencies. Although decreases or absence of several serum proteins were shown, radiopulse-immunoprecipitation studies of albumin and fibrinogen synthesis suggested that the decreased synthesis rates were a secondary defect. Serum glycoproteins were not altered more than other constituents in the mutant material.

摘要

在毛色基因座上因辐射诱导缺失等位基因而纯合的新生小鼠中,已观察到肝脏内质网存在严重的超微结构异常。这些超微结构缺陷伴随着几种酶的缺乏以及血清蛋白水平的降低。开展了血清蛋白合成的研究,以探究合成速率降低,尤其是那些被认为在膜结合核糖体上合成的成分的合成速率降低,是否是这些缺乏的原因。尽管发现了几种血清蛋白减少或缺失,但对白蛋白和纤维蛋白原合成的放射性脉冲免疫沉淀研究表明,合成速率降低是一种继发性缺陷。在突变体材料中,血清糖蛋白的变化并不比其他成分更大。

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